Purpose. The adult brain undergoes activity-dependent plastic modifications during pathological processes, that are reminiscent of those observed during development. For example, seizures induce neuronal loss, neurogenesis, axonal and dentritic sprouting, gliosis and circuit remodelling. Neurotrophic factors, and Fibroblast Growth Factor-2 (FGF-2) in particular, are well-known mediators in each of the above cellular events. Aim of this mini-review is to summarize and discuss the data supporting the idea that FGF-2 may be involved in seizure generation and in their sequelae. Methods. Epilepsy models: kainate and kindling. FGF-2 knock mice; FGF-2 overexpressing mice. Results. 1) Seizures increase FGF-2 mRNA and protein levels in specific brain areas and up-regulate the expression of its receptor FGFR-1. 2) Acute intra-hippocampal injection of FGF-2 cause seizures, while chronic i.c.v. infusion of low dose FGF-2 does not affect kainate seizures but promote behavioural recovery and reduces hippocampal damage. 3) Kainate seizures severity is not altered in FGF-2 knock-out mice, but is increased in FGF-2 over-expressing mice. Conclusions. FGF-2 is implicated in seizure susceptibility and in seizure-induced plasticity.
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