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

• Published in: Journal of neuroinflammation 2010-11, Vol.7 (1), p.81-81, Article 81
• Main Authors: Bovolenta, Roberta, Zucchini, Silvia, Paradiso, Beatrice, Rodi, Donata, Merigo, Flavia, Navarro Mora, Graciela, Osculati, Francesco, Berto, Elena, Marconi, Peggy, Marzola, Andrea, Fabene, Paolo F, Simonato, Michele
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - pharmacology; Colleges & universities; Electroencephalography; Epilepsy; Fibroblast Growth Factor 2 - pharmacology; Fibroblast growth factors; Hippocampus - drug effects; Hippocampus - pathology; Hippocampus - physiopathology; Immunization; Inflammation; Inflammation - pathology; Interleukin-1beta - metabolism; Neurosciences; Physiological aspects; Random Allocation; Rats; Recurrence; Risk factors; Rodents; Seizures (Medicine); Seizures - metabolism; Seizures - pathology; Seizures - physiopathology; Seizures - prevention & control; Short Report; Status Epilepticus - chemically induced; Status Epilepticus - pathology
• ISSN: 1742-2094; 1742-2094
• DOI: 10.1186/1742-2094-7-81

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.