Open Access Short report

Hippocampal FGF-2 and BDNF overexpression attenuates epileptogenesis-associated neuroinflammation and reduces spontaneous recurrent seizures

Roberta Bovolenta12, Silvia Zucchini12, Beatrice Paradiso12, Donata Rodi12, Flavia Merigo3, Graciela Navarro Mora37, Francesco Osculati34, Elena Berto25, Peggy Marconi25, Andrea Marzola6, Paolo F Fabene3 and Michele Simonato12*

Author Affiliations

1 Section of Pharmacology, Department of Clinical and Experimental Medicine, and Neuroscience Center, University of Ferrara, Italy

2 National Institute of Neuroscience, Italy

3 Section of Anatomy, Department of Neurological, Neuropsychological, Morphological and Movement Sciences, University of Verona, Verona, Italy

4 IRCSS "Bonino Pulejo", Messina, Italy

5 Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy

6 Section of Pathology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy

7 Instituto de Neurociencias, CSIC & Universidad Miguel Hernández, San Juan de Alicante, Spain

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Journal of Neuroinflammation 2010, 7:81  doi:10.1186/1742-2094-7-81

Published: 18 November 2010


Under certain experimental conditions, neurotrophic factors may reduce epileptogenesis. We have previously reported that local, intrahippocampal supplementation of fibroblast growth factor-2 (FGF-2) and brain-derived neurotrophic factor (BDNF) increases neurogenesis, reduces neuronal loss, and reduces the occurrence of spontaneous seizures in a model of damage-associated epilepsy. Here, we asked if these possibly anti-epileptogenic effects might involve anti-inflammatory mechanisms. Thus, we used a Herpes-based vector to supplement FGF-2 and BDNF in rat hippocampus after pilocarpine-induced status epilepticus that established an epileptogenic lesion. This model causes intense neuroinflammation, especially in the phase that precedes the occurrence of spontaneous seizures. The supplementation of FGF-2 and BDNF attenuated various parameters of inflammation, including astrocytosis, microcytosis and IL-1β expression. The effect appeared to be most prominent on IL-1β, whose expression was almost completely prevented. Further studies will be needed to elucidate the molecular mechanism(s) for these effects, and for that on IL-1β in particular. Nonetheless, the concept that neurotrophic factors affect neuroinflammation in vivo may be highly relevant for the understanding of the epileptogenic process.