Alterations in Seizure Susceptibility and in Seizure-induced Plasticity after Pharmacologic and Genetic Manipulation of the Fibroblast Growth Factor-2 System
Article first published online: 29 JUN 2005
Volume 46, Issue Supplement s5, pages 52–58, July 2005
How to Cite
Zucchini, S., Barbieri, M. and Simonato, M. (2005), Alterations in Seizure Susceptibility and in Seizure-induced Plasticity after Pharmacologic and Genetic Manipulation of the Fibroblast Growth Factor-2 System. Epilepsia, 46: 52–58. doi: 10.1111/j.1528-1167.2005.01009.x
- Issue published online: 29 JUN 2005
- Article first published online: 29 JUN 2005
- Fibroblast growth factor-2;
- FGF-2 knockout mice;
- FGF-2 overexpressing mice
Summary: Purpose: The adult brain undergoes activity-dependent plastic modifications during pathologic processes that are reminiscent of those observed during development. For example, seizures induce neuronal loss, neurogenesis, axonal and dendritic sprouting, gliosis, and circuit remodeling. Neurotrophic factors and fibroblast growth factor-2 (FGF-2), in particular, are well-known mediators in each of these cellular events. The aim of this minireview is to summarize and discuss the data supporting the idea that FGF-2 may be involved in seizure generation and in their sequelae.
Methods: We used epilepsy models of kainate and kindling, with FGF-2 knockout mice and FGF-2 overexpressing mice.
Results: Seizures increase FGF-2 mRNA and protein levels in specific brain areas and upregulate the expression of its receptor FGFR-1. Short-term intrahippocampal injection of FGF-2 cause seizures, whereas long-term i.c.v. infusion of low-dose FGF-2 does not affect kainate seizures but promotes behavioral recovery and reduces hippocampal damage. Kainate seizure severity is not altered in FGF-2 knockout mice, but is increased in FGF-2 overexpressing mice.
Conclusions: FGF-2 is implicated in seizure susceptibility and in seizure-induced plasticity.